Expert Tips On Wound Bed Preparation

Treating chronic lower extremity ulcerations successfully depends on how well one understands the complex and dynamic interaction of multiple factors that contribute to the slow or non-healing nature of these ulcerations. Wound bed preparation, which is essential to managing difficult ulcerations, involves exudate reduction, appropriate debridement and the reduction of the wound’s bioburden. Indeed, removing the local barriers to healing will prepare the wound bed to support the activities necessary for wound healing. The process of wound bed preparation begins with the initial evaluation of the patient. It’s important to begin with a comprehensive history of the patient’s ulcer/wound. You should get an appreciation of the duration of the ulcer/wound and all of the previous treatments. This history will give you an insight as to what the patient has been going through both physically and emotionally. A thorough history can also help you ascertain whether the patient is compliant with the treatment. You should obtain a thorough medical history as well. Then you should proceed to examine the ulceration. When examining an ulcer, it’s important to compare the ulcerated extremity to the contralateral extremity. One mentor’s favorite quote was one by Thomas Campbell, who said, “Coming events cast their shadow before.” In other words, we can usually get an appreciation of what could have contributed to the ulcer formation by looking at the contralateral extremity, which typically has the same appearance and underlying pathology as the affected extremity. Understanding The Factors That Affect Wound Healing Pinpointing and understanding the underlying etiology of the ulceration is key to arriving at an appropriate treatment course. On many occasions, we see patients whose ulcerations have been treated for months yet they were never told the etiology of the ulcer because the physician was not sure. Granted, there are times when we come across an ulcer that just doesn’t fit into any of the ulcer categories and stumps all of us but these types of ulcerations are very few. In our opinion, one should be able to properly diagnose the slow or non-healing ulcer 99 percent of the time. After making the correct diagnosis, we attempt to identify why the ulcer has not been progressing in a timely fashion. There are several reasons that ulcerations become chronic. In our clinic, if we don’t see signs of ulcer healing after three to four weeks of treatment, we step back and re-evaluate the ulcer. However, it is common to see patients who have had chronic non-healing ulcerations for months and sometimes years. In our experience, infection, inadequate offloading or arterial insufficiency cause these chronic wounds in at least half of the cases we see. The other 50 percent of the ulcerations are more complicated. Some of these causes include but are not limited to edema, elevated levels of proteases in the wound, decreased levels of growth factors, increased levels of inflammatory cytokines and cell senescence. It’s up to the clinician to recognize the contributing factors to the non-healing ulceration and come up with the appropriate treatment protocol. In our clinic, we employ multiple modalities to prepare the wound bed and address the aforementioned reasons for non-healing. Pertinent Pearls On Debriding Tough Ulcerations When it comes to neuropathic ulcerations, debridement is usually the first step as it reduces the bioburden, potentially prevents an infection and allows you to better visualize and inspect the wound. Necrotic tissue is typically characterized by yellow, green or gray, moist and loose tissue. Steed, et. al., reported in their multicenter study that patients who underwent debridement showed an improved healing response compared to the patients who did not undergo debridement.2 Sometimes, necrotic tissue presents as eschar. This black, leathery tissue is a full-thickness necrosis that one may see in patients who have severe arterial insufficiency or in those whose tissues have undergone desiccation. Stable eschars are well adhered to the underlying subcutaneous tissue without any exudate, fluctuance or surrounding cellulitis. An unstable eschar is loose from the underlying tissue, has a boggy feel to it, has underlying exudates and/or surrounding cellulitis. The topic of eschar debridement is a bit controversial. Some physicians and surgeons believe you should debride eschars in order to get rid of the necrotic tissue regardless of whether the eschar is stable. In our clinic, the protocol is to perform sharp debridement of unstable eschar and refrain from debriding stable eschar. In our opinion, debridement is typically necessary in neuropathic and pressure (decubitus) ulcerations. These two types of ulcerations typically present with necrotic or non-viable tissue. On the other hand, venous insufficiency and ischemic (arterial) ulcerations typically do not require debridement. In a great majority of venous ulcers, there is no necrotic tissue. You will see a yellow/green fibrinous film that covers the underlying viable tissue, but this is merely the result of the exudates that dry and cover the healthy underlying tissue. In our clinic, it’s exceptionally rare for us to perform sharp debridement for venous ulcerations. We have found that sharp debridement is very painful in this patient population and do not believe it is necessary in speeding up the healing process. Our protocol is to mechanically debride (saline moistened gauze) the fibrinous film, which is usually easy to remove. If the fibrinous film still remains on the base of the ulcer, we’ll leave it alone and continue with the compression treatment. Venous stasis ulcerations do well on their own, by way of autolytic debridement, provided that you reduce the edema via compression. Arterial ulcerations rarely require debridement unless there is an underlying infection that needs to be drained. It’s important for all of us to realize that arterial disease is not a black and white issue. Peripheral vascular disease (PVD) is a spectrum that extends from mild to moderate to severe disease. Most of our diabetic patients with ulcerations have concomitant PVD. However, a significant majority of them will heal in spite of arterial disease. When an ulcer is diagnosed with an ischemic etiology, it implies there is severe underlying arterial disease. The chances of achieving healing without a revascularization are slim. Therefore, when we say that arterial ulcerations should rarely be debrided, we’re talking about the true arterial ulcers and not the ulcers that have a different etiology with a concomitant, underlying arterial insufficiency. We utilize enzymatic debridement in our clinic. However, it should not be considered a substitute for sharp debridement. We instruct our patients to use the enzymatic debridement agents at home in between clinic visits. This helps to clean up the ulcer base and makes it easier for you to debride without causing significant discomfort and pain to the patient. However, be aware these agents may cause excessive amounts of exudate, which can create irritation of the surrounding skin and lead to possible infection. Essential Insights For Managing Exudate The second step in our management of lower extremity ulcerations is wound exudate. Studies have shown that healing wounds appear to have relatively low levels of inflammatory cytokines and protein-degrading enzymes (proteases). However, non-healing wounds contain very high levels of inflammatory cytokines and proteases. This implies that the exudate in chronic non-healing ulcerations may actually hinder and delay the healing process. When dealing with a chronic ulcer, it doesn’t matter what the etiology is because researchers believe chronic wounds are similar in that they share characteristics such as elevated levels of cytokines and high protease activity.3 Researchers believe the high protease activity, particularly the matrix metalloproteases (MMPs) in chronic ulcerations, degrades growth factors and damages the granulation tissue, both of which are vital in the normal wound repair process. Managing the exudate is an important part of wound bed preparation and can be accomplished in several different ways. In our clinic, we frequently use a foam or an alginate dressing as a primary dressing to absorb some of the exudates in moderate to heavily exudative ulcers. Recently, we became more aggressive in managing heavily exudative ulcerations/wounds by using the VAC (vacuum assisted closure) device. VAC therapy removes interstitial fluid and promotes granulation tissue formation. Indeed, the VAC may be a viable option when you are faced with a chronic, non-healing ulceration. The common remark about the VAC is that one should only use it for deep wounds with a large defect. However, in our clinical experience, one can and should consider the VAC as an option for superficial wounds. Another option for managing exudate is Promogran (Johnson and Johnson), a new product that incorporates oxidized regenerated cellulose with collagen. In-vitro studies have shown this biomaterial reduces the activity of proteases and protects growth factors from degradation. In our clinic, we’re using Promogran as a primary dressing and we’ve seen promising results so far.3 The Ins And Outs Of Edema Edema is the third issue we address in preparing the wound bed. Edema has been associated with an increased risk of ulceration.4 Peripheral edema impairs local blood flow. Therefore, not only does it play a role in ulcer formation, it is also one of the factors which slows the healing rate. One of the most common misconceptions is that you’ll only see edema in patients who have venous insufficiency ulcerations. In our experience, management of edema frequently gets overlooked or is underemphasized in the treatment of foot ulcerations. Almost all of the ulcerations that we deal with have an active inflammatory process and ulcers frequently get stuck in a chronic inflammatory phase of wound healing. When faced with a chronic non-healing ulcer, one should realize the edema is present around the ulceration whether there is pitting edema or not. After appropriate debridement, we apply a compression dressing (Profore, Dynaflex or Unna boot). Final Notes Wound bed preparation is a combination of debridement, exudate management and edema control. In a great majority of patients who have chronic ulcers, these three techniques are enough to create a healthy viable granulation tissue ulcer base which is ready for epithelialization. Sometimes, oral antibiotics are needed to reduce bacterial burden. However, all of these techniques would be moot if the ulcer were inadequately offloaded (see “Key Pointers On Offloading Techniques” above). These techniques of wound bed preparation have been successfully applied in our day to day treatment and management of difficult to heal ulcerations. The products mentioned in this article are ones that we use in the clinic. Certainly, other products are available and may have a place within the treatment algorithm. Dr. Reyzelman is the Chairman of the Department of Medicine at the California College of Podiatric Medicine and practices privately in San Francisco. Dr. Tidwell is a first-year resident at the Veterans Affairs Medical Center in Albuquerque, N.M.
 

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References 1. APhA drug treatment protocols: management of foot ulcers in patients with diabetes. J Am Pharm Assoc. 2000;40:467-474. 2. Steed DL, et al. Effect of Extensive Debridement and Treatment on Healing of Diabetic Foot Ulcers. J Am Coll Surgeons. 1996; 183:61-64. 3. Cullen B, et. al. Mechanism of action of PROMOGRAN, a protease modulating matrix, for the treatment of diabetic foot ulcers. Wound Rep Reg 2002;10:16-25. 4. Mast BA, et. al. Interactions of Cytokines, Growth Factors, and Proteases in Acute and Chronic Wounds. Wound Rep Reg 1996;4:411-20. 5. Reiber GE, et. al. Causal Pathways for Incident Ulcers in Patients with Diabetes from Two Settings. Diabetes Care 1999;22:157-62. 6. Armstrong D, Stacpoole-Shea S. TCC and removable cast walkers/mitigation of plantar heel pressure. JAPMA 1999; 89(1):50-53. 7. Fleischli J, Lavery L, Vela S, Ashry H, Lavery D. Comparison of strategies for decreasing pressure of neuropathic ulcers. JAPMA 1997; 87(10):446-472.